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  • Injured RGCs are known to undergo early functional deficits [17,36-38], including alterations in their axoplasmic flow properties [26,39-43], in several metabolic functions such as diminutions of their Thy-1 mRNA levels [36,44-46], or induction of phagocytic activity in microglia [47,48], and in the regulation of a substantial number of genes [49,50] including the downregulation of Brn3a [51] shortly before cell death.
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